Movement Disorders (revue)

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Dopaminergic regulation of olfactory type G-protein α subunit expression in the striatum.

Identifieur interne : 004289 ( Ncbi/Merge ); précédent : 004288; suivant : 004290

Dopaminergic regulation of olfactory type G-protein α subunit expression in the striatum.

Auteurs : I. Ruiz-Dediego [Espagne] ; J R Naranjo [Espagne] ; D. Hervé [Espagne] ; R. Moratalla [Espagne]

Source :

RBID : pubmed:25772224

Abstract

In rodents, the olfactory type G-protein α subunit (Gαolf) couples the dopamine D1 receptor (D1R) to adenylyl cyclase, triggering intracellular signaling and neuronal activation. In the striatum, Gαolf is enriched in the striosomes. Changes in Gαolf protein levels have been observed after dopamine depletion. However, the regulation of Gαolf expression by dopamine and dopamine receptors is not fully understood.

DOI: 10.1002/mds.26197
PubMed: 25772224

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<title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<div type="abstract" xml:lang="en">In rodents, the olfactory type G-protein α subunit (Gαolf) couples the dopamine D1 receptor (D1R) to adenylyl cyclase, triggering intracellular signaling and neuronal activation. In the striatum, Gαolf is enriched in the striosomes. Changes in Gαolf protein levels have been observed after dopamine depletion. However, the regulation of Gαolf expression by dopamine and dopamine receptors is not fully understood.</div>
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<Year>2015</Year>
<Month>07</Month>
<Day>16</Day>
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<ISSN IssnType="Electronic">1531-8257</ISSN>
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<Volume>30</Volume>
<Issue>8</Issue>
<PubDate>
<Year>2015</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
<ISOAbbreviation>Mov. Disord.</ISOAbbreviation>
</Journal>
<ArticleTitle>Dopaminergic regulation of olfactory type G-protein α subunit expression in the striatum.</ArticleTitle>
<Pagination>
<MedlinePgn>1039-49</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26197</ELocationID>
<Abstract>
<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">In rodents, the olfactory type G-protein α subunit (Gαolf) couples the dopamine D1 receptor (D1R) to adenylyl cyclase, triggering intracellular signaling and neuronal activation. In the striatum, Gαolf is enriched in the striosomes. Changes in Gαolf protein levels have been observed after dopamine depletion. However, the regulation of Gαolf expression by dopamine and dopamine receptors is not fully understood.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">To address this, Striatal Gαolf expression pattern was studied in wild-type and genetically engineered mice lacking D1R, D2R (D2 receptor), and downstream regulatory element antagonist modulator (DREAM) protein whose dopamine levels were manipulated. Dopamine depletion was accomplished by 6-hydroxydopamine (6-OHDA) or by Pitx3 ablation, and dopamine replacement by chronic levodopa (l-dopa). The Gαolf levels were analyzed by immunohistochemistry, Western blot, and real-time quantitative polymerase chain reaction (RT-qPCR).</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Our results demostrate that Dopamine depletion or inactivation of D1R abolished the striosomal pattern of Gαolf expression and increased Gαolf protein levels. Dopamine replacement in wild-type lesioned mice reestablished both the expression pattern and protein levels, but paradoxically increased Gαolf messenger RNA (mRNA). In D1R(-/-) mice, dopamine depletion decreased striatal Gαolf expression, whereas l-dopa did not restore either Gαolf levels or its expression pattern. Inactivation of D2R or changes in the cAMP/PKA signaling pathway downstream of Gαolf did not modify its expression.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Our results show a homeostatic, negative regulation of Gαolf by dopamine and by D1R stimulation, which are also required for the striosomal Gαolf pattern. These results shed light on the regulation of Gαolf by dopamine signaling that could be involved in the pathophysiology of the maladaptive response to chronic l-dopa treatment in Parkinson's disease.</AbstractText>
<CopyrightInformation>© 2015 International Parkinson and Movement Disorder Society.</CopyrightInformation>
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<LastName>Ruiz-DeDiego</LastName>
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<Affiliation>CIBERNED, Instituto de Salud Carlos III, CIBERNED, Madrid, Spain.</Affiliation>
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<Affiliation>Centro Nacional de Biotecnología, CSIC, Madrid, Spain.</Affiliation>
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<AffiliationInfo>
<Affiliation>Institut du Fer à Moulin, CIBERNED, Madrid, Spain.</Affiliation>
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<Affiliation>Université Pierre et Marie Curie, Paris, France.</Affiliation>
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<Keyword MajorTopicYN="N">AIMs</Keyword>
<Keyword MajorTopicYN="N">Parkinson's disease</Keyword>
<Keyword MajorTopicYN="N">dopaminergic receptors</Keyword>
<Keyword MajorTopicYN="N">l-dopa</Keyword>
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